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Tobacco and other drugs

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Tobacco and other drugs

An association between tobacco and other drug use has been well established. The nature of this association remains unclear. The two main theories are the phenotypic causation (gateway) model and the correlated liabilities model. The causation model argues that smoking is a primary influence on future drug use, while the correlated liabilities model argues that smoking and other drug use are predicated on genetic or environmental factors.

Causation model

A 1994 report from the Center on Addiction and Substance Abuse at Columbia University, found a correlation between the use of cigarettes and alcohol and the subsequent use of cannabis. The report asserted a link between alcohol and cannabis use and the subsequent use of illicit drugs like cocaine.[1] It found that when younger children used, the more often they use them, the more likely they were to use cocaine, heroin, hallucinogens and other illicit drugs. The report concludes that the data is already robust enough to make a strong case to step up efforts to prevent childhood use of cigarettes and to take firm steps to reduce children’s access to these "gateway drugs".[2]

[4]

In 2002, the RAND Drug Policy Research Center released a paper on one of their studies stating that it "casts doubt on claims that marijuana acts as a "gateway" to the use of cocaine and heroin, challenging an assumption that has guided U.S. drug policies since the 1950s."[5] These findings of the RAND Drug Policy Research Center's study are in contradiction to the claims made by NIDA.

Correlative model

Genetic correlation

Smoking may have a genetic predisposing factor; one 1990 study posited that 52% of the variance in smoking behaviour is attributable to heritable factors,[6] and another in 1962 on identical twins found that only 21% of participant pairs were discordant (one smoking, one non-smoking), also suggesting a genetic basis or at least a genetic susceptibility or predisposition. This, however, does not demonstrate the genetic susceptibility to smoke, as there may be confounding factors e.g. stronger correlation between personality and smoking would suggest the genetic predisposition is instead towards personality. In addition, most twin studies utilize a small sample size of separated twins—the result is a sample population of twins who lived in the same environment, considerably overestimating the genetic connection. To date, there is no conclusive evidence.

See also

References

  1. ^ Cigarettes, Alcohol, Marijuana: Gateways to Illicit Drug Use, Center on Addiction and Substance Abuse at Columbia University, October 1994, retrieved 17 July 2007
  2. ^ Betty Ford Center - Dr. James West Public Q&A Page. URL Accessed October, 2006
  3. ^ The National Institute on Drug Abuse (NIDA), part of the NIH, a component of the U.S. Department of Health and Human Services. - Nicotine Craving and Heavy Smoking May Contribute to Increased Use of Cocaine and Heroin - Patrick Zickler, NIDA NOTES Staff Writer. URL Accessed October, 2006
  4. ^ RAND | News Release | RAND Study Casts Doubt on Claims That Marijuana Acts as "Gateway" to the Use of Cocaine and Heroin
  5. ^ RAND | News Release | RAND Study Casts Doubt on Claims That Marijuana Acts as "Gateway" to the Use of Cocaine and Heroin
  6. ^ Swan GE, Carmelli D, Rosenman RH, et al. Smoking and alcohol consumption in adult male twins: genetic heritability and shared environmental influences. J Subst Abuse. 1990;2(1):39–50. PMID 2136102

External links

  • CORK Bibliography: Gateway Hypothesis
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